Concise review

for
clinicians
Clinical
Pearls
in Cardiology

Clinical Pearls in Cardiology

Stephen L. Kopecky, MD, and Scott C. Litin, MD

t the 2001 annual conference of the American College

of Physicians, a new teaching format to aid physician
learning, Clinical Pearls, was introduced. Clinical Pearls is
designed with the 3 qualities of physician-learners in mind.
First, we physicians enjoy learning from cases. Second, we
like concise, practical points that we can use in our practice. Finally, we take pleasure in problem solving.
In the Clinical Pearls format, speakers present a number
of short cases in their specialty to a general internal medicine
audience. Each case is followed by a multiple-choice question answered live by attendees using an audience response
system. The answer distribution is shown to attendees. The
correct answer is then displayed and the speaker discusses
teaching points, clarifying why one answer is most appropriate. Each case presentation ends with a Clinical Pearl,
defined as a practical teaching point that is supported by the
literature but generally not well known to most internists.
Clinical Pearls is currently one of the most popular sessions at the American College of Physicians meeting. As a
service to its readers, Mayo Clinic Proceedings has invited
a selected number of these Clinical Pearl presentations to
be published in our Concise Reviews for Clinicians section.
Clinical Pearls in Cardiology is one of them.

a severe cough in multiple previous trials of these agents.

He denies any peripheral edema, orthopnea, or paroxysmal nocturnal dyspnea.

Case 1

Question
Which one of the following is the most reasonable next
step in the management of this patient?
a. Prescribe a statin such as rosuvastatin, 5 mg/d
b. Refer him to a cardiologist to be evaluated for an automatic implantable cardioverter-defibrillator (AICD)
c. Refer him to a cardiologist to be evaluated for cardiac
resynchronization therapy
d. Initiate treatment with hydralazine and long-acting
nitrates
e. Increase furosemide to 80 mg/d

A 51-year-old man with dilated cardiomyopathy whom

you have been treating for the past 3 years has class II
New York Heart Association (NYHA) heart failure (slight
limitation of physical activity, can perform activities of
daily living, can walk >2 blocks or climb >1 flight of
stairs). Prior coronary angiography showed normal coronary arteries. He would like to be more active and asks
if there is anything else that could be tried. He has been
taking 100 mg/d of metoprolol and has had a resting heart
rate of 58 beats/min. He has never been able to tolerate
either an angiotensin-converting enzyme inhibitor (ACEI)
or an angiotensin II receptor blocker (ARB), developing

From the Division of Cardiovascular Diseases (S.L.K.) and Division of General

Internal Medicine (S.C.L.), Mayo Clinic, Rochester, MN.
See end of article for correct answers to questions.
Individual reprints of this article are not available. Address correspondence
to Stephen L. Kopecky, MD, Division of Cardiovascular Diseases, Mayo Clinic,
200 First St SW, Rochester, MN 55905 (kopecky.stephen@mayo.edu).
2010 Mayo Foundation for Medical Education and Research

Mayo Clin Proc.

May 2010;85(5):473-478

Medications
Metoprolol, 100 mg/d
Furosemide, 20 mg/d
Eplerenone, 50 mg/d
Digoxin, 0.125 mg/d
Findings
Electrocardiography. Sinus rhythm with PR interval of
147 ms and QRS interval of 98 ms
Echocardiography. Left ventricular ejection fraction
(LVEF), stable at 42%; no significant valve disease; dilated
left ventricle with global hypokinesis
Examination. Jugular venous pressure, 8 cm above the
center of the right atrium (upper end of normal range);
blood pressure, 137/76 mm Hg; heart rate, 58 beats/min;
lungs clear; no peripheral edema
Cardiac Examination. Positive S3 present; 1/6 systolic
ejection murmur at the left lower sternal border that decreases with Valsalva maneuver; enlarged and sustained
point of maximum impulse

Discussion
Hydralazine and isosorbide dinitrate have been shown to
be beneficial in patients intolerant of ACEIs or ARBs.1 This
combination was shown to be more beneficial than placebo
and comparable to enalapril in the early Department of
Veteran Affairs studies.2 Recent updates have shown the
benefit of hydralazine and isosorbide dinitrate when added
to ACEIs or ARBs in African Americans.3 Doses should
initally be low and then be up-titrated as tolerated to 50
mg of hydralazine 4 times daily and 40 mg of isosorbide

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Clinical Pearls in Cardiology

dinitrate 3 times daily. In general, ACEIs and ARBs are

used because adherence to a combined regimen of hydralazine and isosorbide dinitrate has been poor as a result of
the large number of tablets required and adverse effects
such as headaches that occur in some patients. A combined
regimen of hydralazine and isosorbide dinitrate is a good
option when ACEIs or ARBs cannot be used because of
cough, hyperkalemia, or renal insufficiency. However, no
trials have evaluated the use of this combination therapy in
a population of patients who are intolerant of ACEIs and
ARBs. In the current guidelines, this is a class IIb recommendation, meaning that it may be considered but is not
without risk and that further studies are needed.
The patient's LVEF is high enough (>35%) that he does
not meet criteria for an AICD and has no history of sudden
cardiac death or ventricular tachycardia. He has a normal
QRS interval and would not benefit from resynchronization therapy. Digoxin has been shown to be helpful in
symptom relief in class III but not in class II patients.
The patient's fluid status appears to be optimal, and so he
is unlikely to benefit from an increased dose of diuretic
agents.
Clinical Pearl
Hydralazine and isosorbide dinitrate can be effective
therapy in patients unable to tolerate ACEIs and ARBs or
in African Americans with heart failure.
Case 2
A 76-year-old man presents with shortness of breath on
exertion that began 6 months ago and has since gradually worsened. He states that he can no longer perform
normal activities without developing symptoms and that
climbing more than one flight of stairs causes him to be
profoundly short of breath, requiring him to stop and rest.
When walking on level ground, he does well, but any hill
causes dyspnea. He has a history of hypertension but no
history of hyperlipidemia, diabetes, tobacco abuse, or
family history of early coronary artery disease. He is taking no medications.
Findings
Electrocardiography. Normal sinus rhythm with normal intervals and no significant abnormality
Chest Radiography. Normal cardiac silhouette with
clear lung fields
Echocardiography. LVEF, 64% with normal valves
and normal left and right ventricular size and function; no
regional wall motion abnormalities; normal wall thickness
Stress Test. Ability to walk for 4.8 min on Bruce protocol (78% of predicted functional aerobic capacity); heart
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May 2010;85(5):473-478

rate, increased to 146 beats/min; blood pressure, 200/98

mm Hg; stopped test because of dyspnea; negative electrocardiographic findings for ischemia
Examination. Lungs clear; jugular venous pressure,
elevated at 12 cm above the right atrium; peripheral edema,
1+; body mass index, 32 kg/m2
Question
Which one of the following actions would be least appropriate for this patient?
a. Initiate treatment with an ACEI for blood pressure
b. Initiate treatment with a diuretic agent to resolve his
congestion and peripheral edema
c. Recommend a regular exercise program, telling him to
start low and increase gradually
d. Encourage him to lose weight
e. Refer him for coronary angiography
Discussion
The patient has heart failure with preserved ejection fraction (HFPEF). Recently, this entity has been shown to account for almost half of patients with symptoms of heart
failure, specifically those with dyspnea on exertion, peripheral edema, or orthopnea. The long-term outcome (ie,
mortality) of these patients is very similar to that of patients
with decreased ejection fraction.
Heart failure with preserved ejection fraction is a
particular problem in elderly patients. The prevalence of
symptoms of heart failure increases from 3% in those aged
65 years to more than 80% in those older than 80 years.
Heart failure is the most common reason for hospitalization
in elderly patients, and the diagnosis of HFPEF is inadequately recognized and treated because both patients and
physicians frequently attribute these symptoms to aging
when echocardiography shows normal systolic function.4
Clinicians should always be alert to this diagnosis.
Although HFPEF can be associated with infiltrative
diseases such as amyloidosis or, most commonly, with
hypertension, it is also seen in patients with deconditioning, obesity, or coronary artery disease risk factors such
as hyperlipidemia or diabetes. Patients with hypertension
should be treated and volume overload appropriately managed. However, despite multiple randomized trials, no evidence suggests that patients without hypertension or fluid
overload benefit from taking an ACEI, ARB, or -blocker.5
Stress testing revealed no evidence of coronary artery disease in this patient. He has no significant risk factors, and
coronary angiography is not indicated. Weight loss and a
regular exercise program have been shown to be beneficial
for symptoms; however, they do not necessarily reduce
hospitalizations or major adverse cardiac events. Obesity
is in the differential diagnosis along with hypertension.

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Clinical Pearls in Cardiology

Clinical Pearl
Accounting for one-half of all heart failure cases, HFPEF
should be considered in patients (especially elderly patients)
with unexplained dyspnea on exertion. In terms of long-term
outcome and treatment, HFPEF is similar to heart failure
with decreased ejection fraction.6
Case 3
A 66-year-old woman with known coronary artery disease has had 2 previous myocardial infarctions (MIs),
the first 7 years previously and the second 11 months
previously. After her last MI, her ejection fraction was
documented to be 28%. She currently has class II NYHA
heart failure.
Medications
Lisinopril, 40 mg/d
Carvedilol, 12.5 mg twice daily
Aldosterone, 25 mg/d
Aspirin, 81 mg/d
Pravastatin, 20 mg/d
Findings
Laboratory Tests. Sodium, 138 mEq/L (to convert
to mmol/L, multiply by 1); potassium, 4.4 mmol/L;
creatinine, 1.2 mg/dL (to convert to mol/L, multiply by
88.4)
Echocardiography. Ejection fraction, 32% with mild
mitral regurgitation; a markedly enlarged left ventricle with
anterior wall hypokinesis
Electrocardiography. Heart rate, 60 beats/min with
sinus rhythm; PR interval, 168 ms; QRS interval, 111 ms;
corrected QT interval, 402 ms; prior anterior MI
Examination. Blood pressure, 116/72 mm Hg; heart
rate, 60 beats/min and regular; jugular venous pressure,
flat; no peripheral edema; lungs clear with good breath
sounds at both bases
Cardiac Examination. Presence of S3 with an enlarged point of maximum impulse that is bifid; no murmur
or rub
Question
Which one of the following would be the best therapy for
this patient?
a. Given that she has NYHA class II heart failure, con-
tinue current therapy
b. Add in a diuretic agent such as furosemide, 20 mg/d
c. Add in digoxin, 0.125 mg, every 6 hours for 4 times,
0.125 mg/d orally
d. Refer for cardiac resynchronization therapy
e. Refer for evaluation for an AICD
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Discussion
This patient with class II NYHA heart failure is doing
quite well and is already taking all the recommended
medications, including those for afterload reduction
(ACEIs/ARBs), good doses of b-blocker (metoprolol
or carvedilol), and an aldosterone-inhibiting diuretic
agent (spironolactone or eplerenone). A diuretic agent
is not indicated because her examination revealed no
peripheral edema or congestion. Digoxin is not indicated
because the patient's functional class II heart failure is
stable. Because her QRS interval is of normal width, it is
unlikely that she would benefit from cardiac resynchronization therapy, which should be considered in patients
with left bundle branch block or a widening QRS interval.7 To further evaluate the need for cardiac resynchronization therapy, echocardiography can be performed to
evaluate dyssynchrony of the ventricular contraction.
However, the American Society of Echocardiography
guidelines suggest that echocardiography criteria not
be used as part of the selection criteria for cardiac resynchronization therapy. The patient's ejection fraction
has been depressed (<35%) for 11 months while she
was receiving good medical therapy, and so she would
meet indications for an AICD, which has been shown to
decrease mortality more than routine care and/or antiarrhythmic therapy.8
Indications for AICD
Ischemic heart failure with prior MI and LVEF <35%.
Nonischemic heart failure with LVEF <35% for at least 9
months while receiving good medical therapy
Documented episode of cardiac arrest due to ventricular
fibrillation, not due to transient or reversible cause
Documented sustained ventricular tachycardia, either
spontaneous or induced by an electrophysiology
study; not associated with an acute MI and not due to
a transient or reversible cause
Documented familial or inherited conditions with a high
risk of life-threatening ventricular tachycardia, such as
long-QT syndrome or hypertrophic cardiomyopathy
with a family history of sudden cardiac death. Exclusion criteria are NYHA class IV heart failure, cardiogenic shock, coronary artery bypass grafting or percutaneous coronary intervention in the past 3 months,
a documented need for revascularization, irreversible
brain damage, or anticipated survival of <1 year
Clinical Pearl
In patients with heart failure and prolonged depression of
LVEF (<35%) while receiving optimal medical management, AICD has been shown to decrease mortality and
should be considered.

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Clinical Pearls in Cardiology

Case 4
A 68-year-old man follows up with you after a hospitalization 2 weeks previously for an episode of acutely decompensated heart failure. During the hospitalization, he had
undergone diuresis with intravenous furosemide to eliminate
4.5 kg (10 lb) of fluid. He has decreased left ventricular function, thought to be secondary to chronic mitral regurgitation.
The patient's mitral valve had been repaired 2 years ago, but
his ejection fraction of 42% has not improved significantly
since then. He has a dilated left ventricle and has symptoms
characteristic of functional NYHA class II heart failure.
The patient has trouble adhering to a sodium- and
fluid- restricted diet. He lives alone and cooks his own food
and tends to eat high-sodium items despite having been
instructed by the dietitian many times not to do so.
Medications
Furosemide, 20 mg in the morning
Metoprolol, 25 mg/d
Lisinopril, 10 mg at bedtime
Findings
Laboratory Tests. Creatinine, 1.4 mg/dL; estimated
glomerular filtration rate, 46 mL/min/1.73 m2 (reference
range, >60 mL/min/1.73 m2); potassium, 4.5 mmol/L;
clear lung fields with enlarged cardiac silhouette on cardiac
radiography
Examination. Height, 177 cm; weight, 99 kg; blood
pressure, 118/76 mm Hg; heart rate, 62 beats/min and
regular; both lung bases clear; no edema in the extremities
Cardiac Examination. Enlarged bifid; lateral point
of maximal impulse; 1/6 holosystolic murmur at the apex
that decreases with Valsalva maneuver; positive S3; no S4;
jugular venous pressure, 8 cm above the right atrium
Question
Which one of the following is the next best step in the treatment of this patient?
a. Increase dose of lisinopril to 20 mg/d
b. Add 30 mg of isosorbide mononitrate in the morning
and increase to 60 mg as tolerated
c. Refer to a dietitian for a low-sodium, fluid-restricted
(1500 mL) diet
d. Request that he weigh each morning; provide a
schedule for increasing furosemide if he gains weight
e. Refer him to an electrophysiologist for possible AICD
implantation
Discussion
It has been shown that 76% of patients who are hospitalized for acute decompensated heart failure have a history
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of heart failure. A substantial increase in extracellular

fluid volume may occur without evidence of peripheral
edema or pulmonary congestion. An increase in selfreported body weight has been shown to occur about 11
days before a hospital admission for acute decompensated
heart failure and about 3 days before the onset of dyspnea.
Compared with a mean increase in weight of less than .91
kg (<2 lb), a weight gain between .91 and 2.3 kg (2-5 lb)
is associated with an odds ratio (OR) of increased risk
of hospitalization for heart failure of 2.8; between 2.3 to
4.5 kg (5-10 lb), with an OR of 4.5; and greater than 4.5
kg (10 lb), with an OR of 7.7.9 When a patients weight
increases by more than .91 kg (2 lb) in a day or 2.3 kg
(5 lb) overall, it is beneficial to have the patient either
call the nurse for instructions for increasing the dose of
diuretic agents or double the furosemide dose for 3 days.
The dose of supplemental potassium should be increased
during this time.
Clinical Pearl
Increases in body weight are associated with hospitalization for heart failure and begin at least 1 week before
admission. Identifying weight gain and treating it by
increasing the dose of diuretic agents have been shown
to be effective in reducing hospitalizations due to acute
decompensated heart failure.10
Case 5
A 73-year-old woman with left ventricular systolic dysfunction whom you have been treating for several years
presents to the emergency department. She is having
palpitations and is diagnosed as having atrial fibrillation
(heart rate, 130 beats/min) in the emergency department. She denies chest pain but is mildly short of breath
with a rapid ventricular rate. The patient is not sure how
long she has been having palpitations; she thinks they
have been intermittent during the past few months but
have always resolved after a few minutes. This episode,
however, lasted for more than 2 hours, prompting her to
seek treatment.
Medical History
Hypertension well controlled with hydrochlorothiazide
History of hypothyroidism treated medically with nor-
mal findings on sensitive thyroid-stimulating homone
test
No history of bleeding problems, strokes, or transient
ischemic attacks
No syncope or presyncope
Known coronary artery disease with 3-vessel coronary
artery bypass graft performed 11 years previously

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Clinical Pearls in Cardiology

Medications
Hydrochlorothiazide, 25 mg/d
Lisinopril, 20 mg/d
Metoprolol, 12.5 mg/d
Aspirin, 81 mg/d
Social history
Not physically active
Lives in a high-rise retirement complex
Findings
Labortory Tests. Sensitive thyroid-stimulating hormone
test, normal; electrolyte levels, normal; complete blood cell
count, normal; troponin level, normal
Electrocardiography. Atrial fibrillation; old inferolateral MI; no acute ST-T changes
Echocardiography. Biatrial enlargement with enlarged
left ventricle and decreased function; ejection fraction, 34%;
evidence of prior inferolateral MI
Examination. Height, 167 cm; weight, 63 kg; lungs
clear; rhythm, irregularly irregular; 1/6 systolic ejection
murmur at the lower left sternal border; no edema
Question
Which one of the following is the best therapy for this
woman with systolic left ventricular dysfunction presenting with atrial fibrillation?
a. Control heart rate with b-blockers and/or digoxin
and provide anticoagulation with warfarin to an international normalized ratio of 2 to 3
b. Administer antiarrhythmic propafenone and perform
direct-current cardioversion
c. Administer antiarrhythmic propafenone, perform trans-
esophageal echocardiography to rule out left atrial
thombus, and perform direct-current cardioversion
d. Refer to an electrophysiologist for consideration of
atrioventricular node ablation with pacemaker implantation and long-term anticoagulation
e. Refer to an electrophysiologist for pulmonary vein isolation ablation to eradicate the atrial fibrillation
Discussion
The best option is to control the patient's heart rate with bblockers and/or digoxin and to provide anticoagulation with
warfarin to an international normalized ratio of 2 to 3.
A 2008 study evaluated the hypothesis that patients
with heart failure and atrial fibrillation need to be returned
to sinus rhythm.11 The long-held belief was that patients
with heart failure particularly needed their atrial kick to
help their cardiac output and that patients with low ejection
fraction should be returned to sinus rhythm. However, in
this large study, no benefit was achieved by returning these
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May 2010;85(5):473-478

patients to sinus rhythm. Patients prescribed class 1 antiarrhythmic agents were found not to respond favorably and
were predisposed to proarrhythmic effects.12 Class 3 antiarrhythmic agents, such as sotalol, dofetilide, and amiodarone, can maintain sinus rhythm in some patients; however, treatment with these agents is associated with increased
risk of organ toxicity (amiodarone) and proarrhythmic
effects (dofetilide). Returning a patient to sinus rhythm has
not been shown to obviate the need for long-term anticoagulation. Therefore, the best option is to control heart rate
and recommend long-term anticoagulation. If controlling
the heart rate is not possible, the next best option would be
to consider atrioventricular node ablation with permanent
pacemaker implantation; these patients would still need to
continue anticoagulation therapy. Patients with an enlarged
left atrium have less long-term benefit from the encircling
atrial fibrillation ablation.
Clinical Pearl
Even in patients with heart failure and atrial fibrillation,
heart rate control combined with anticoagulation therapy is
the preferred first-line treatment for atrial fibrillation.
Case 6
A 78-year-old woman whom you have been treating for the
past 10 years for chronic functional NYHA class III heart
failure (ejection fraction, 28%) was admitted to the hospital
3 days previously for an episode of heart failure. A year
earlier, she had an AICD/cardiac resynchronization device
implanted. Since being admitted to the hospital, she has undergone diuresis (3.6 kg [8 lb]) and feels much better. You
are ready to dismiss her today, with instructions to continue
her usual home regimen of medications: furosemide, 20
mg; potassium 20 mmol/L; carvedilol, 25 mg twice a day;
and lisinopril, 20 mg in the evening. The patient weighs
herself daily and takes extra furosemide and potassium
when her weight increases. She is currently adhering to a
low-sodium diet with a 1500-mL fluid restriction. Her level
of the N-terminal fragment of probrain-type natriuretic
peptide (NT-proBNP) is 2186 pg/mL (to convert to ng/L,
multiply by 1) (optimal for those >75 years, 1800 pg/mL).
The etiology of her heart failure is coronary artery disease,
but her last stress test 4 months previously showed a fixed
anterior defect but no evidence of ischemia.
Question
Which one of the following would be the best treatment
option for this patient at this point in her care?
a. Continuation of current therapy
b. Addition of an aldosterone inhibitor, such as spironolactone or eplerenone

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Clinical Pearls in Cardiology

c. Augmentation of current therapy to reduce her NTproBNP levels to normal and her functional status to
NYHA class II or less
d. Switch from carvedilol to metoprolol
e. Follow-up stress test
Discussion
Addition of an aldosterone antagonist is recommended in
patients with moderately severe to severe symptoms of
heart failure (NYHA class III-IV) and reduced LVEF.13
An initial dose of 12.5 mg of spironolactone or 25 mg
of eplerenone is recommended; if appropriate, the dose
may be increased to 25 mg of spironolactone or 50 mg of
eplerenone.
Levels of creatinine should be 2.5 mg/dL or less in men
and 2.0 mg/dL or less in women, and potassium levels
should be less than 5 mmol/L without a history of severe
hyperkalemia. If monitoring the potassium or renal function is not feasible, then the risks may outweigh the benefits
of aldosterone agents. Such therapy is not currently recommended without concomitant diuretic therapy in patients
with chronic heart failure. Nonsteroidal anti-inflammatory
drugs and cyclooxygenase-2 inhibitors should be avoided.
The risk of hyperkalemia is increased with concomitant use
of higher doses of ACEIs (captopril 75 mg/d; enalapril or
lisinopril, 10 mg/d). The risk of hyperkalemia increases
progressively when serum creatinine exceeds 1.6 mg/
dL. In elderly patients or others with low muscle mass in
whom the serum creatinine level does not accurately reflect glomerular filtration rate, it should be determined that
glomerular filtration rate or creatinine clearance exceeds 30
mL/min. Diarrhea or other causes of dehydration should be
addressed emergently.
Metoprolol has not been shown to be superior to
carvedilol for treatment of patients with heart failure.
Using standard medical therapy to treat to a NYHA class
II or less heart failure has been compared to using it to
achieve that goal and to lower NT-proBNP or BNP levels.
Lowering the BNP or NT-proBNP levels has consistently
been shown not to add benefit above that achieved by
treating patients to NYHA class II or less heart failure.13
Therefore, it is not recommended that BNP levels be followed up regularly for treatment. However, BNP levels
have been helpful in making a diagnosis for patients
with unexplained dyspnea (who commonly present to the
emergency department). Also, a BNP level of less than
600 pg/mL at the time of hospital discharge for acute decompensated heart failure correlates with a lower recurrent
cardiovascular event rate.14,15

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Clinical Pearl
Addition of aldosterone inhibitors has been recommended
for patients with NYHA class III or IV heart failure to reduce symptoms and morbidity. Treating patients to achieve
a certain BNP or NT-proBNP level does not help prevent
recurrent episodes of acute decompensated heart failure
any more than treating to symptoms of NYHA class II
heart failure.

References
1. Cohn JN, Johnson G, Ziesche S, et al. A comparison of enalapril with
hydralazine-isosorbide dinitrate in the treatment of chronic congestive heart
failure. N Engl J Med. 1991;325:303-310.
2. Loeb HS, Johnson G, Henrick A, et al; V-HeFT VA Cooperative Studies
Group. Effect of enalapril, hydralazine plus isosorbide dinitrate, and prazosin
on hospitalization in patients with chronic congestive heart failure. Circulation. 1993;87:VI78-VI87.
3. Taylor AL, Ziesche S, Yancy C, et al. Combination of isosorbide dinitrate
and hydralazine in blacks with heart failure. N Engl J Med. 2004;351:20492057.
4. Owan TE, Hodge DO, Herges RM, Jacobsen SJ, Roger VL, Redfield
MM. Trends in prevalence and outcome of heart failure with preserved ejection
fraction. N Engl J Med. 2006;355:251-259.
5. Yusuf S, Pfeffer MA, Swedberg K, et al. Effects of candesartan in patients with chronic heart failure and preserved left-ventricular ejection fraction:
the CHARM-Preserved Trial. Lancet. 2003;362:777-781.
6. Kupari M, Lindroos M, Iivanainen AM, Heikkila J, Tilvis R. Congestive
heart failure in old age: prevalence, mechanisms and 4-year prognosis in the
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7. Bardy GH, Lee KL, Mark DB, et al. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. N Engl J Med.
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8. Moss AJ, Zareba W, Hall WJ, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N
Engl J Med. 2002;346:877-883.
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of weight change preceding hospitalization for heart failure. Circulation.
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10. Schiff GD, Fung S, Speroff T, McNutt RA. Decompensated heart
failure: symptoms, patterns of onset, and contributing factors. Am J Med.
2003;114:625-630.
11. Roy D, Talajic M, Nattel S, et al. Rhythm control versus rate control for
atrial fibrillation and heart failure. N Engl J Med. 2008;358:2667-2677.
12. Boos CJ, Carlsson J, More RS. Rate or rhythm control in persistent atrial
fibrillation? QJM. 2003;96:881-892.
13. Pitt B, Zannad F, Remme WJ, et al. The effect of spironolactone on
morbidity and mortality in patients with severe heart failure. N Engl J Med.
1999;341:709-717.
14. Jessup M, Abraham WT, Casey DE, et al. 2009 focused update: ACCF/
AHA guidelines for the diagnosis and management of heart failure in adults:
a report of the American College of Cardiology Foundation/American Heart
Association Task Force on Practice Guidelines developed in collaboration
with the International Society for Heart and Lung Transplantation. Circulation. 2009;119(14):1977-2016.
15. Januzzi JL, van Kimmenade R, Lainchbury J, et al. NT-proBNP testing
for diagnosis and short-term prognosis in acute destabilized heart failure: an
international pooled analysis of 1256 patients: the International Collaborative
of NT-proBNP Study. Eur Heart J. 2006;27:330-337.

Correct answers: Case 1: d, Case 2: e, Case 3: e, Case 4: d, Case

5: a, Case 6: b

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